Systemic inflammatory response syndrome (SIRS) and organ dysfunction make it challenging to predict which major trauma patients are at risk of developing sepsis. Additionally, the unclear pathogenesis of sepsis after trauma contributes to its high morbidity and mortality. Identifying early predictive and diagnostic biomarkers, as well as exploring related metabolic pathways, is crucial for improving early prevention, diagnosis, and treatment. This study prospectively analyzed plasma samples from patients with severe trauma collected between March 2022 and November 2023. Trauma patients were divided into two groups based on whether they developed sepsis within two weeks: the TDDS group (trauma patients who did not develop sepsis) and the TDS group (trauma patients who did develop sepsis). Plasma samples from the TDS group were collected at the time of sepsis diagnosis (Sepsis group). Metabolite concentrations were measured using ultrahigh-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) through untargeted metabolomics. From the differential metabolites between the TDS and TDDS groups, we identified five significant metabolites (all area under the curve (AUC) ≥ 0.94) as early predictive biomarkers for sepsis after trauma: (1) docosatrienoic acid, (2) 7-alpha-carboxy-17-alpha-carboxyethylandrostan lactone phenyl ester, (3) sphingomyelin (SM) 8:1;2O/26:1, (4) N1-[1-(3-isopropenylphenyl)-1-methylethyl]-3-oxobutanamide, and (5) SM 34:2;2O. Furthermore, five significant metabolites (all AUC ≥ 0.85) were identified as early diagnostic biomarkers from the comparison between the TDS and TDDS groups: (1) lysophosphatidylcholine (LPC) O-22:1, (2) LPC O-22:0, (3) uric acid, (4) LPC O-24:2, and (5) LPC 22:0-SN1. 26 metabolites shared between two comparisons (TDS vs. TDDS and sepsis vs. TDS) were identified. Of which, 19 metabolites belong to lipid metabolism. The top three metabolic pathways related to sepsis after trauma under the impact of severe trauma were: (1) glycerophospholipid metabolism, (2) porphyrin metabolism, and (3) sphingolipid metabolism. The top three metabolic pathways related to sepsis after trauma under the impact of infection were: (1) caffeine metabolism, (2) biosynthesis of unsaturated fatty acids, and (3) steroid hormone biosynthesis. Our study identified early predictive and diagnostic biomarkers and explored metabolic pathways related to sepsis after trauma. These findings provide a foundation for future research on the onset and development of sepsis, facilitating its early prevention, diagnosis, and treatment based on specific metabolites and metabolic pathways.

Acute pain is always the most common complaint in Emergency Department admissions and options for analgesia are limited. Nitrous oxide/oxygen possess many properties showing it may be an ideal analgesic method for the Emergency Department; it is quick-acting, well-tolerated, and does not mask signs and symptoms. The aim of this study is to evaluate the safety and analgesic effect of the fixed nitrous oxide/oxygen mixture for trauma patients in a busy emergency environment. The randomized, double-blind, prospective, placebo-controlled study will be carried out in the Emergency Department of General Hospital of Ningxia Medical University. The target research objects are trauma patients who present to the Emergency Department and report moderate to severe intensities of acute pain. A total of 90 patients will be recruited and randomly assigned into the treatment and control group. The treatment group will receive conventional pain treatment plus nitrous oxide/oxygen mixture and the control group will receive conventional pain treatment plus oxygen. Neither patients, nor investigators, nor data collectors will know the nature of the gas mixture in each cylinder and the randomization list. Outcomes will be monitored at baseline(T0), 5 min (T1), and 15 min (T2) after the beginning of intervention and at 5 min post intervention (T3) for each group. The primary outcome is the level of pain relief after the initial administering of the intervention at T1, T2, and T3. Secondary outcomes include adverse events, physiological parameters, total time of the gas administration, satisfaction from both patients and healthcare professionals, and the acceptance of patients. Our previous studies suggested that a fixed nitrous oxide/oxygen mixture was an efficacious analgesic for the management of burning dressing pain and breakthrough cancer pain. The results of this study will provide a more in-depth understanding of the effect of this gas. If this treatment proves successful, it could help to generate preliminary guidelines and be implemented widely in trauma patients with pain in Emergency Departments. Chinese Clinical Trial Register, ChiCTR-INR-16007807 . Registered on 21 January 2016.

Objective: To describe the clinical characteristics, treatments, and outcomes of tetanus and determine the most appropriate focus for tetanus prevention and treatment to reduce morbidity and mortality in China. Methods: Four databases, including the Chinese Bio-Medical Literature Database, Chinese National Knowledge Infrastructure, Chinese Scientific Journal Database, and Wan-fang Data, were searched from 1 January, 2000 to 30 October, 2022. Results: In total, 151 articles including 6084 tetanus patients met the inclusion criteria. Additionally, 5925 patients had their gender recorded in detail, among which 66.67% (3950/5925) were male, and 33.33% (1975/ 5925) were female. The average age in the detailed records was reported in 4773 cases, with an overall average age of 46.69. The number of patients’ places of residence was 580. Those from rural areas comprised the highest percentage with 88.62% (514 / 580). The causes of injury were recorded in 1592 cases in total; injuries caused by metals, wood, and wooden spikes accounted for the highest percentage with 54.52% (868/1592). Patient outcomes were recorded in 4305 cases, with a mortality of 9.34% (402/4305). The leading causes of death included treatment terminated by family members, asphyxia due to persistent spasms, respiratory failure, and autonomic dysfunction, family automatic abandonment and asphyxia accounted for the highest percentage, both 24.00% (54/225). Conclusion: The overall success rate of tetanus treatment in China has dramatically improved, but the prevention and control of non-neonatal tetanus is still challenging. Focus should be placed on the prevention of adult tetanus and standardizing the use of sedative and spasmolytic drugs. Additionally, medical professionals should popularize tetanus prevention and treatment knowledge among the people and strengthen training in grass-roots hospitals.

Aims: This study aimed to evaluate the effects of VC on SIMI in rats. Methods: In this study, the survival rate of high dose VC for SIMI was evaluated within 7 days. Rats were randomly assigned to three groups: Sham group, CLP group, and high dose VC (500 mg/kg i.v.) group. The animals in each group were treated with drugs for 1 day, 3 days or 5 days, respectively. Echocardiography, myocardial enzymes and HE were used to detect cardiac function. IL-1β, IL-6, IL-10 and TNF-α) in serum were measured using ELISA kits. Western blot was used to detect proteins related to apoptosis, inflammation, autophagy, MAPK, NF-κB and PI3K/Akt/mTOR signaling pathways. Results: High dose VC improved the survival rate of SIMI within 7 days. Echocardiography, HE staining and myocardial enzymes showed that high-dose VC relieved SIMI in rats in a time-dependent manner. And compared with CLP group, high-dose VC decreased the expressions of pro-apoptotic proteins, while increased the expression of anti-apoptotic protein. And compared with CLP group, high dose VC decreased phosphorylation levels of Erk1/2, P38, JNK, NF-κB and IKK α/β in SIMI rats. High dose VC increased the expression of the protein Beclin-1 and LC3-II/LC3-I ratio, whereas decreased the expression of P62 in SIMI rats. Finally, high dose VC attenuated phosphorylation of PI3K, AKT and mTOR compared with the CLP group. Significance: Our results showed that high dose VC has a good protective effect on SIMI after continuous treatment, which may be mediated by inhibiting apoptosis and inflammatory, and promoting autophagy through regulating MAPK, NF-κB and PI3K/AKT/mTOR pathway.

Sepsis after trauma and trauma-induced SIRS have similar symptoms, making their differentiation challenging. Therefore, biomarkers are needed to differentiate between sepsis after trauma and trauma-induced SIRS. We hypothesized that sepsis following trauma induces distinct alterations in blood metabolism compared to trauma-induced SIRS and sought to identify metabolite biomarkers in blood that could differentiate between the two. In this retrospective study, the existing blood metabolomics data from 60 patients without trauma-induced SIRS, 40 patients with trauma-induced SIRS, and 50 non-trauma control cases were analyzed. Among 40 traumatic patients with SIRS, 16 developed sepsis (SDS group), 24 did not develop sepsis (SDDS group) within the subsequent two-week period after trauma. A pairwise comparison between SDS group and SDDS group was used to screen the differential metabolites as biomarkers distinguishing sepsis after trauma from trauma-induced SIRS. Using partial least‑squares discriminant analysis, we demonstrated that SDS group was metabolically distinct from the SDDS group. A total of 37 differential metabolites were found between SDS group and SDDS group. We selected 5 most significantly different metabolites between SDS and SDDS groups as biomarkers to discriminate sepsis after trauma from trauma-induced SIRS, which were 7-alpha-carboxy-17-alpha-carboxyethylandrostan lactone phenyl ester, docosatrienoic acid, SM 8:1;2O/26:1, SM 34:2;2O, and N1-[1-(3-isopropenylphenyl)-1-methylethyl]-3-oxobutanamide. Our study has identified the potential of these biomarkers for differentiating sepsis after trauma from trauma-induced SIRS. This not only provides a new approach for the early diagnosis of sepsis after trauma but also lays a solid foundation for further research based on targeted metabolomics, which may lead to the development of more effective treatment strategies in the future.

Background: Elderly trauma (ET) carries a high mortality rate due to comorbidities, frailty, and limited physiological reserve. Understanding its specific pathophysiology is essential for enabling precision treatment. Objective: To identify characteristic metabolic dysregulations and specific pathways in geriatric trauma. Methods: We retrospectively analyzed existing metabolomics data from ET, young and middle-aged trauma (YMAT), elderly controls (EC), and young and middle-aged controls (YMAC). Results: An IVD integrating 8 significant metabolic pathways (SMPs) from ET vs EC and 10 SMPs from YMAT vs YMAC identified 3 pathways specific to ET: glyoxylate and dicarboxylate metabolism, galactose metabolism, and Pantothenate and coenzyme A (CoA) biosynthesis. The second IVD integrating these pathways with 3 SMPs from EC vs YMAC identified 2 metabolic pathways specific to ET independent of natural aging: glyoxylate and dicarboxylate metabolism, and pantothenate and CoA biosynthesis. Finally, the third IVD integrating them and 7 SMPs from ET vs YMAT identified glyoxylate and dicarboxylate metabolism as unique signature of geriatric trauma. Conclusion: This study was one of few metabolomics studies that distinguish between geriatric trauma-related metabolic changes and baseline aging factors, and revealed glyoxylate and dicarboxylate metabolism disorder as a key pathway specific to geriatric trauma. Understanding it may inform the development of age-tailored strategies for improving trauma outcomes in the elderly.